As shown in Figure 5E and F, inhibition of ERK or JNK significantly attenuated ABT-263-induced Mcl-1Thr163 phosphorylation and Mcl-1 accumulation, suggesting that the phosphorylation of Mcl-1Thr163 may contribute to ERK- and JNK-mediated Mcl-1 stabilization upon ABT-263 treatment in HCC cells. The gene discussed is MCL1; the disease is hepatocellular carcinoma.